%0 Journal Article %T 促性腺激素释放激素和多巴胺对虹鳟(Oncorhynchus mykiss)离体脑垂体细胞分泌促性腺激素的影响 %T Effects of Gonadotropin-releasing Hormone (GnRH) and Dopamine on Gonadotropin (GTH) Secretion from in vitro Pituitary Cells of Rainbow Trout %A 侯亚义 %A HOU,Yayi %J 湖泊科学 %J Journal of Lake Sciences %@ 1003-5427 %V 13 %N 1 %D 2001 %P 51-56 %K 虹鳟;促性腺激素;促性腺激素释放激素;多巴胺;脑垂体细胞 %K Rainbow trout;gonadot ropin;gonadot ropin-releasing hormone (GnRH);dopamine;pituitary cell %X 本文研究了不同性腺发育时期淡水饲养的雌雄虹鳟(Oncorhynchus mykiss)血浆促性腺激素(GTH)浓度的变化规律;以及在离体条件下,探讨了促性腺激素释放激素(GnRH)、GnRH拮抗物和多巴胺对虹鳟脑垂体细胞分泌促性腺激素(GTH -Ⅱ)的影响.结果表明:(1)在雄性,血浆中GTH-Ⅱ的水平随性腺发育而逐渐增高;在雌性,仅排卵期血浆中GTH-Ⅱ的水平明显增高.(2)未成熟期和成熟期的雌性虹鳟脑垂体细胞对sGnRH和cGnRH刺激的敏感性表现不尽相同.成熟期和排卵后的脑垂体细胞对GnRH的刺激较为敏感,GTH -Ⅱ的分泌量较多.(3)在没有sGnRH的存在下,GnRH拮抗物对GTH -Ⅱ的分泌不发生作用,而在sGnRH的存在下,GnRH拮抗物对GTH -Ⅱ的分泌表现出浓度依赖的抑制作用.(4)在没有sGnRH的存在下,多巴胺对GTH-Ⅱ的分泌不发生作用,而当多巴胺的浓度一定时,随着sGnRH浓度的增加,GTH -Ⅱ分泌的量增大.另外,不论sGnRH还是cGnRH都不影响不同时期的脑垂体细胞GTH -Ⅰ的分泌.这些结果可为虹鳟的人工催产提供一些理论依据. %X Plasma gonadotropin (GTH)levels during immature, mature and ovulated periods and effects of gonadot ropin-releasing hormone (GnRH)and dopamine on GTH secret ion of in vitro pituitary cells of rainbow trout were investigated.Plasma GTH levels increased wi th gonadal development.The different effects of sGnRH and cGnRH on GTH-Ⅱ secretions of pitui tary cells in vitro f rom immature, mature and ovulated periods of rainbow trout w ere observed.GnRH antagonist did not change GTH-Ⅱ contents under the absence of sGnRH w hile GnRH antagonist suppressed dose-dependently GTH-Ⅱ secretions of pi tuitary cells in combination with sGnRH. Dopamine also did not affect GTH-Ⅱ levels under the absence of sGnRH, while G TH-Ⅱ secretions of pituitary cells were enhanced w hen the dosage of sGnRH was increased with the presence of constant levels of dopamine.In addition, sGnRH and cGnRH had no effects on GTH-Ⅰ secretions.These result s provide some basic informations for modulating the spontaneous release of GTH-Ⅱ and cont rolling fish reproduction. %R 10.18307/20010108 %U http://www.jlakes.org/ch/reader/view_abstract.aspx %1 JIS Version 3.0.0